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    CSF hydrothorax after ventriculoperitoneal shunt without catheter migration: a case report
    (SPRINGER, 2011) Kocaogullar, Yalcin; Guney, Onder; Kaya, Bulent; Erdi, Fatih
    Ventriculoperitoneal (VP) shunting is the most common procedure performed for the management of hydrocephalus. VP shunt related complications remain a persistent problem in current clinical practice. Five-year-old female patient was admitted to our hospital with persistent dyspnea complaint. The patient was operated at the age of 3 months and a VP shunt established in a different clinic due to hydrocephalus associated with Dandy-Walker malformation. The patient's chest X-ray revealed right sided pleural effusion. Thorasentesis was performed and the effusion was drained with a chest tube. The discharged liquid was consistent with CSF. Scintigraphic radionuclide shunt analyses were performed and CSF passage from abdomen to chest and lower mediastinal region was determined in the late static images. The patient was operated and the incorporated ventriculoperitoneal shunt was removed. Hydrothorax was completely resolved after early postoperative stage. CSF hydrothorax especially without catheter migration is an unusual but potentially serious-clinical complication.
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    The Effects of Alpha Lipoic Acid on Cerebral Vasospasm Following Experimental Subarachnoid Hemorrhage in the Rabbit
    (TURKISH NEUROSURGICAL SOC, 2011) Erdi, Mehmet Fatih; Guney, Onder; Kiyici, Aysel; Esen, Hasan
    AIM: The aim of this study is to determine the effects of a strong dithiol antioxidant, alpha lipoic acid (ALA) on cerebral vasospasm following subarachnoid hemorrhage in a rabbit model. MATERIAL and METHODS: Twenty-one New Zealand white rabbits were assigned to one of three groups: group 1 (control), group 2 (SAH only), group 3 (SAH+ALA). ALA was administered (100 mg/kg/day, single dose, intraperitoneally). The rabbits were sacrificed 72 hours after SAH. The basilar artery lumen areas, arterial wall thickness and endothelial apoptosis in a cross section of basilar artery were measured in all groups. The tissue MDA, SOD, GSH-Px levels were also determined. RESULTS: The elevated tissue MDA levels after SAH were significantly reduced by ALA treatment. The reduced tissue SOD and GSH-Px levels after SAH were also elevated by ALA treatment. In the treatment group the average wall thickness and the mean percentages of apoptotic cells (apoptotic index) were reduced and the average cross-sectional areas of the basilar artery were increased statistically significantly. CONCLUSION: ALA treatment attenuates the severity of cerebral vasospasm by its strong antioxidant, antivasospastic and antiapoptotic properties. ALA may potentially serve as agents in the prevention of cerebral vasospasm after SAH.
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    Electrophysiology of papillary muscle in SAH: changes and N-acetylcysteine protection
    (SPRINGER, 2009) Ayaz, Murat; Guney, Onder; Erdi, Fatih; Kucukbagriacik, Yusuf
    Although subarachnoid hemorrhage (SAH) serves as a good model to study heart-brain interactions, neither the changes on the single ventricular action potential (SVAP) and contraction nor the effects of possible cardioprotective agents have been investigated. A total of 18 male rabbits were used for the three experimental groups. SAH was induced by replacing the cerebrospinal fluid (CSF) with fresh autologous blood at the ratio of 1 mL to the 1-kg body mass (N = 6). In the control (CON; N = 6) group, the CSF was replaced with serum physiologic at the same ratio. The treated SAH group (SAH+NAC) received daily intraperitoneal N-acetylcysteine (NAC; 150 mg/kg for 3 days) starting from just before SAH was induced by CSF replacement. On the fourth day, animals were examined for the single action potential and contraction recordings from the left ventricular papillary muscle. At the end of 3 days, the overshoot decreased together with increased time to reach the peak potential. Additionally, the resting membrane potential was depressed and repolarization was slowed during SVAPs. On the other hand, peak tension depressed and time to peak increased. NAC treatment, which protects infarction in the brain, prevented these pathological changes in the cardiac muscle. SAH-induced cardiac changes can be attributed to adenosine triphosphate depletion through mitochondrial dysfunction. Pretreatment of NAC to SAH on the other hand had a positive effect on these cardiac changes. But the exact mechanism by which NAC treatment protects the cardiac muscle needs further investigation.